Troxerutin protects hippocampal neurons against amyloid beta-induced oxidative stress and apoptosis

Authors

  • Fereshteh Farajdokht Neurosciences Research Center (NSRC), Tabriz University of Medical Sciences, Tabriz, Iran
  • Mohammad Amani Drug Applied Research Center of Tabriz University of Medical Sciences, Tabriz, Iran
  • Fariba Mirzaei Bavil Drug Applied Research Center of Tabriz University of Medical Sciences, Tabriz, Iran
  • Alireza Alihemmati Drug Applied Research Center of Tabriz University of Medical Sciences, Tabriz, Iran
  • Gisou Mohaddes Drug Applied Research Center of Tabriz University of Medical Sciences, Tabriz, Iran
  • Shirin Babri Neurosciences Research Center (NSRC), Tabriz University of Medical Sciences, Tabriz, Iran

DOI:

https://doi.org/10.17179/excli2017-526

Keywords:

Alzheimer's disease, amyloid beta, acetylcholinesterase, oxidative stress

Abstract

Alzheimer's disease (AD) is an age-related neurodegenerative disease linked with increased production and/or deposition of amyloid-beta (Aβ) in the brain. The aim of the present study was to investigate the possible neuroprotective effect of troxerutin on an animal model of Alzheimer's disease. Alzheimer model was induced by a single dose intracerebroventricular (ICV) injection of Aβ 1-42 (5 nmol/5 µl). Thereafter, troxerutin (300 mg/kg) was gavaged for 14 days. The hippocampal malondialdehyde (MDA) levels and enzymatic activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), and acetylcholinesterase (AChE) were measured using enzyme-linked immunosorbent assay (ELISA) method. In addition, the number of apoptotic cells in the dentate gyrus (DG) was assessed by TUNEL kit. The results showed that ICV microinjection of Aβ 1-42 increased MDA levels, reduced SOD and GPx, and increased AChE activities in the hippocampus. Chronic administration of troxerutin significantly attenuated MDA levels and AChE activity and increased SOD and GPx activities in the hippocampus. Moreover, the number of apoptotic cells was decreased by troxerutin treatment. Taken together, our study demonstrated that troxerutin could increase the resistance of hippocampal neurons against apoptosis, at least in part, by diminishing the activity of AChE and oxidative stress. Therefore, troxerutin may have beneficial effects in the management of Alzheimer's disease.

Downloads

Published

2017-08-09

How to Cite

Farajdokht, F., Amani, M., Mirzaei Bavil, F., Alihemmati, A., Mohaddes, G., & Babri, S. (2017). Troxerutin protects hippocampal neurons against amyloid beta-induced oxidative stress and apoptosis. EXCLI Journal, 16, 1081–1089. https://doi.org/10.17179/excli2017-526

Issue

Vol. 16 (2017)

Section

Original articles

License

Authors who publish in this journal agree to the following terms:

  • The authors keep the copyright and grant the journal the right of first publication under the terms of the Creative Commons Attribution license, CC BY 4.0. This licencse permits unrestricted use, distribution and reproduction in any medium, provided that the original work is properly cited.
  • The use of general descriptive names, trade names, trademarks, and so forth in this publication, even if not specifically identified, does not imply that these names are not protected by the relevant laws and regulations.
  • Because the advice and information in this journal are believed to be true and accurate at the time of publication, neither the authors, the editors, nor the publisher accept any legal responsibility for any errors or omissions presented in the publication. The publisher makes no guarantee, express or implied, with respect to the material contained herein.
  • The authors can enter into additional contracts for the non-exclusive distribution of the journal's published version by citing the initial publication in this journal (e.g. publishing in an institutional repository or in a book).

Most read articles by the same author(s)